Background/Purpose: Rheumatoid Arthritis (RA) is an autoimmune disease characterized by articular inflammation, cartilage and bone alterations and is commonly associated with chronic pain difficult to treat with currents therapies. Target Nerve Growth Factor (NGF), a specific neurotrophin involved in initiation and maintenance of pain, has been already considered as a promising treatment of rheumatoid arthritis symptoms. But, due to the pleiotropic action of NGF, target this neurotrophin conducts to substantial sides’ effect. Our aim is to better understand the involvement of specific intracellular signaling pathways activated by the NGF receptor, the tyrosine kinase type A (TrkA), in the pathophysiology of RA and associated pain symptoms in order to find a more specific modulator downstream NGF. Methods: We performed a multimodal study in knock-in TrkA/C mice expressing a chimeric receptor composed by the native extracellular part of TrkA and the functional transmembrane and intracellular part of the tyrosine kinase type C receptor (TrkC) of the neurotrophin 3 (NT3). We have followed in adjuvant induced-arthritis mice model nociceptive behavior such as mechanical allodynia using von Frey test and thermal hyperalgesia using paw immersion test. In vivo alterations were analyzed with scintigraphic imaging with 99mTc-NTP 15-5 and 99mTc-HMDP, two specific radiotracers of cartilage and bone remodeling respectively. Results: Our results showed a specific decrease of mechanical allodynia without affecting thermal hyperalgesia in TrkA/C monoarthritic mice. This pain modulation was associated with a decrease of 99mTc-HMDP accumulation in the pathologic paw but no difference concerning 99mTc-NTP 15-5 accumulation in TrkA/C mice compared to WT mice. Conclusion: The present study demonstrates a specific involvement of NGF/TrkA signaling in pain, especially mechanotransduction and an impact of the NGF/TrkA signaling pathways modulation on bone remodeling in inflammatory arthritis.